Remember that the absolute risk of this complication for any one mother is quite low, but the fact that the risk is increased at all is a good reason to be cautious about the overuse of cesareans on a population-wide basis.

If you would like to read a more complete summary of this study (and others like it which examined the same question), please read Henci Goer's analysis of the study over at Science & Sensibility.

Introduction: To examine the relationship between first birth by cesarean and antepartum fetal death in a subsequent pregnancy in a large, hospital-based population.

Methods : Data for this retrospective cohort study were taken from a database of all women who gave birth at Brigham and Women's Hospital during 4 waves of data collection beginning in 1994 and ending in 2002. We calculated the risk of antepartum fetal death in the subsequent pregnancy for women whose first birth was by cesarean compared to women with a vaginal first birth. Survival analysis was used to examine the influence of gestational age at birth.

Results: Of 10,996 women who met inclusion criteria, 22% (n = 2450) had first births by cesarean, and 78% (n = 8546) had vaginal first births. The risk of antepartum fetal death in the subsequent pregnancy for women whose first birth was by cesarean was significantly greater than the risk for women whose first birth was vaginal (odds ratio 2.6; 95% confidence interval, 1.1-6.2). The relationship between first birth cesarean and antepartum fetal death in a subsequent pregnancy differed by gestational age at birth, with no excess risk among women with a previous cesarean birth who gave birth before 34 weeks' gestation but with a substantially increased risk for women who gave birth at 34 or more weeks' gestation (unadjusted hazard ratio = 5.6; 95% confidence interval, 1.6-19.8). Hazard ratio estimates for the association remained significant in bivariate models when adjusted for maternal height, weight, age, hypertension, and diabetes.

Discussion: In these data, first birth by cesarean was associated with an increased risk of antepartum fetal death in a subsequent pregnancy. Our findings suggest that antepartum fetal deaths in subsequent pregnancies might be prevented by avoiding primary cesarean birth.

Tuesday, April 17, 2012

As everyone and their mothers have heard by now, a new study just out is promoting the idea that maternal "obesity" is associated with an increased risk for the development of autism in children.

So now even the increase in autism over the years is fat people's fault too, eh? Well, I beg to differ. There are a lot of problems with the study, its conclusions, and how it is being promoted in the media. Quelle surprise.

Science Sensationalism

This is yet another case of Science By Press Release, and frankly, it's appalling. It's yet another way the medical establishment tries to shame fat women out of procreating unless they lose weight first.

Yes, there are risks associated with obesity and pregnancy and it's important to be aware of them, but it's another thing entirely to bludgeon women with them in a way that shames or scares them inappropriately, or paints the choice of a fat women to have a baby as utterly irresponsible.

If you take a look at the study and the way it's been reported, you will find that there are a number of problems. Let's discuss a few of these.

Jumping to Conclusions

Frankly, the public promotion of this finding was very inappropriate because this is the first time scientists have found a relationship between obesity and autism.

One of the prime rules for researchers is that study findings must be corroborated by other studies before being accepted as a true relationship. If this is the first time they have found this relationship, it should have been confirmed by other studies before being publicized.

Since I'm not an expert in the autism field, I did a little digging around to see if other studies have examined the question. One major review of autism literature found that researchers have largely not investigated the topic before. They noted that there was one study which did not find an association between obesity and autism, but that they could not include this study in their review because its findings had not been replicated.

So the study that exonerates obesity doesn't get any press, but the one that finds a connection gets a huge media tour of the world? The one that didn't find an association doesn't even get listed with a reference, only rates a passing mention in a major review, simply because it hasn't been replicated....but the one that does find an association is somehow worthy of huge press attention, even though it hasn't been replicated either? Double standard much?

Although this new finding is interesting on a purely scientific basis, it is not yet something that should be promoted in the media, where people will jump to conclusions about a relationship before it is really proven. Yet that is precisely what has happened, and you can bet it's going to be on every future Scare Provider Risk List for obesity and pregnancy, despite its unconfirmed nature. It's just one more weapon with which to bludgeon women of size around their childbearing choices.

An Alternative Agenda?

That the authors publicized this finding so strongly now, before it has been corroborated elsewhere, suggests another agenda. Either the authors are trying to promote their careers by making a splash with this in the media, or the authors are strongly pushing a public health weight loss agenda. Or perhaps it could be a little bit of both?

What an amazing coincidence that the lead author is a doctoral candidate at U.C. Davis, isn't it? A little publicity for a widely-received research finding goes a long way to grease the thesis process, and maybe even the job-finding prospects afterwards, eh?

Judging by some of the press release comments along the lines of, "Well, we can't say for sure obesity causes autism, but this is just another reason to 'get healthy' before pregnancy," they are hitting the weight loss agenda hard when publicizing the study:

Since more than one-third of U.S. women of child-bearing age are obese, the results are potentially worrisome and add yet another incentive for maintaining a normal weight, said researcher Paula Krakowiak, a study co-author and scientist at the University of California at Davis.

The implication is that if you dare to not achieve that "normal" weight before pregnancy, you are irresponsible and a burden to society with your "damaged" babies.

These days, so much of "science" is all about the public health spin you put on findings.

A Less-Than-Overwhelming Association

Another concern is that the finding was not even that strong. If the study had found a huge relationship between obesity and autism, that might have been grounds for publicity even on a first finding of such a correlation, but it really didn't find that strong a relationship.

The study found that children of obese women had an odds ratio of 1.67 for being on the autism spectrum. In the press releases, this is phrased as "67% higher risk of autism than the children of normal-weight moms." While this cannot be dismissed, it is hardly a really striking finding. If there's really a strong relationship, you want to see a much more dramatic risk increase than that. This "relationship" is fairly tepid at best. It can't be overlooked at this point, but it's certainly not so strong that it really deserved the publicity hype it got.

And if there was really a strong relationship between metabolic conditions in pregnancy and developmental disorders, you would expect that both diabetes and hypertension would come back as risk factors. Indeed, they did, but the confidence interval for these findings crossed 1.0, meaning that those findings could be due simply to coincidence. The confidence interval for the obesity or "any metabolic condition" did not quite cross 1.0, but the fact that both the diabetes and hypertension findings did raises the question of whether this relationship will really hold up in further studies.

And that's the bottom line, isn't it? This finding needs to be replicated in other studies. Promoting it so widely and so overwhelmingly on the basis of such tepid findings is embarrassingly premature.

Causality versus Correlation

As others have pointed out, just because two things happen at the same time doesn't mean they are causally related to each other. Yet many of the press releases trumpet a "parallel rise" in both obesity and autism in recent years, implying causality, although they always insert a token sentence or two that no conclusions can be reached yet:

Although nobody can say the nation's rising obesity rate is to blame for the prevalence of autism, Krakowiak said the parallel increases did catch her attention.

Way to imply causality without actually stating outright that the two are related.

Dr. Daniel Coury, chief of developmental and behavioral pediatrics at Nationwide Children's Hospital in Columbus, Ohio, said the results “raise quite a concern.” He noted that U.S. autism rates have increased along with obesity rates and said the research suggests that those figures may be more than a coincidence.

So let's look at this claim a little further. Several press releases point out that "autism is up 78% since 2002." And the final sentence of the study abstract states, "With obesity rising steadily, these results appear to raise serious public health concerns."

Except that recent data has NOT shown obesity to be rising steadily. It did for a while, and then it leveled off...around the year 2000. Yet autism seems to be rising steadily, with no leveling off of cases, as you might expect if obesity and autism were causally linked.

This doesn't mean we can disprove a link between autism and obesity, just that citing a parallel increase in both obesity and autism doesn't hold up logically, since obesity has leveled off and is not currently increasing.

Again, the authors seem to be most interested in promoting the obesity hysteridemic, rather than looking at actual data in an objective fashion. They've bought into the party line that obesity is increasing at exponential rates and shows no sign of slowing, and they show no willingness to question this meme, nor does the press.

This is sensationalism, not science.

Disorder or Difference?

Another concern for me in the press coverage was the rampant ableism that goes unquestioned in the articles.

Is autism really a "disorder" or is it merely a difference? Is it something that needs to be "fixed", or is it simply a representation of neurological biodiversity?

Do we really need to treat folks on the autism spectrum like a freak show? Or is this just another Public Health Boogeyman to scare people with?

Possible "Causes" of Autism

This study is just the latest in a series of studies promoting a new and trendy "cause" for the Autism Boogeyman.

If you look back over the last several decades, the media is full of these reports. And every few years, something new is blamed (including air pollution, vaccines, MSG, GMOs, pesticides, lead exposure, low vitamin D, and many others). The Autism Blame Game is a common media theme.

After all these reports over the years, blaming yet another possible cause for autism, you'd think that the media would be more cynical and wary of yet another new claim. But each new "cause" is embraced and promoted as THE answer. Obesity is just the latest one, but one that will no doubt stick around a long time because it fits the anti-obesity scare mantra that doctors and the media want to promote.

Mother-Blaming 101

A few decades ago, it was the mother's "frigid" behavior that was blamed for autism, the appalling "Refrigerator Mother" theory. Researchers noticed a difference in interaction between mothers and their children with autism, and blamed "cold" mothers for the development of autism. But what happened was that the mothers were responding to the cues of the child, as mothers do. If hugging or touching your child distresses him greatly, then it is only natural for the mother to decrease that behavior in the best interests of her child. It is an act of love, a response that recognizes and acknowledges the needs of the child over her own. Yet researchers in a notoriously mother-blaming era interpreted it in an entirely different way.

Sadly, such mother-blaming behavior is still happening, only now it is being focused on what mothers do "wrong" in pregnancy.

Given their world view that autism is a disorder, it is understandable the researchers are anxious to figure out its causes, but researchers need to be very careful not to simply indulge in a new and more insidious type of mother-blaming.

Other Physical Causes

Clearly, the most important factor involved in autism is genetics. Twin studies and family history studies have shown that autism is highly heritable, and that genetics is far more important than environmental influences. However, studies on identical twins suggest that sometimes environmental influences are also a factor. In all likelihood, autism is mostly genetic, but may also involve complex interactions between genetics and environmental factors. If it does, the question is which environmental factors?

Many different factors have been tied to autism in research. The ones that seem to have the most credible research behind them include prematurity, older age of parents (especially the father), jaundice after birth, low birth-weight/small-for-gestational-age (LBW/SGA), being the first-born child, bleeding during pregnancy, breech malpositions, maternal use of medication during pregnancy, the mother having been born abroad, gestational diabetes, maternal infection, etc.

However, it's one thing to find a possible association in a data dredge study, and another thing for that factor to be supported in study after study after study. Often something is found to be a factor in one study but not another. It is only when multiple studies consistently find common risk factors that public health actions should be taken. Anything more is premature and ill-considered.

Another problem is that the studies looking at risk factors for autism are subject to considerable methodological variation, with different diagnostic criteria, comparison groups, sample sizes, and methods of assessing autism. Therefore, it is important to be cautious about over-interpreting the results of any one study. It is the big picture that is the most important one.

One meta-analysis acknowledged the weaknesses of most autism studies, saying:

Few factors have been examined in multiple well-conducted studies. Therefore, attempted replication in methodologically strong studies remains necessary. Although the majority of factors examined in multiple studies have given inconsistent results, the preponderance of findings overall have not been statistically significant.

Some research suggests that perhaps it takes multiple "insults" to increase the risk for autism. This includes problems during the pregnancy, problems during the birth, problems in early childhood, and missed developmental markers. This is an interesting theory; it may be that looking for the "magic bullet" is the wrong approach, but rather it is the interaction of several factors (together with a strong genetic predisposition) that is important.

Whatever the answer is, it is clear that many things have been blamed for autism over the years, but that any findings must be interpreted with great caution.

But What If There Is A True Relationship?

Of course, we can't just dismiss the findings of this study totally. The authors did find a relationship, and we can't just dismiss every study with a conclusion we don't like. So let's take a moment to discuss the possibilities.

IF there's a real relationship (which is by no means proven at this point), where do researchers need to go from here to investigate this topic more thoroughly?

Refine the Research

First, the researchers need to stop using obesity as a surrogate for a metabolic abnormality. That assumption is problematic since many obese people do not have diabetes, insulin resistance, or hypertension, and many thin people do. Making obesity an automatic surrogate for metabolic aberration is far too simplistic and leads to overgeneralization of risk.

The picture is likely much more complex and needs to be treated as such. Separate out the obese people with metabolic issues from those without, then compare them to "normal" weight people with and without metabolic issues too. Try and tease out where the true risk factors lie rather than draw broad generalizations.

Second, do follow-up research. If children of obese mothers do turn out to be at increased risk, then why do most obese women not have children with autism?

Compare the pregnancies of fat women whose children developed autism to the pregnancies of fat women whose children did not develop autism. Did those who developed autism have more medical complications in pregnancy? More prematurity? More SGA babies? More gestational diabetes? Evidence of fetal hypoxia at birth? More exposure to pitocin? More cesareans? More epidurals? More iron-deficiency or other nutritional deficits? More inadequate weight gain?

In other words, look deeper than just obesity. Stop being so simplistic, refine the research further, and ask more meaningful questions.

Track Real-Life Incidence Numbers

It's always frustrating when obesity researchers use odds ratios to talk about various risks associated with obesity and pregnancy, which tends to inflate the sense of risk around a complication. Fortunately, the authors of this study at least try to place the risk in some numerical context. One press release noted:

On average, women face a 1 in 88 chance of having a child with autism; the results suggest that obesity during pregnancy would increase that to a 1 in 53 chance, the authors said.

1 in 53 would mean that nearly 2% of all babies born to fat women would be autistic. Notice that they don't document that 2% of all children of fat women are autistic, they just extrapolate and estimate the risk. Frankly, it seems high to me; I don't think that 2% of all the children of fat women I have met are autistic. But we need real data in order to know this for sure, not just extrapolation of risk.

Future research needs to do some long-term follow-up of the children of obese women to see how many really are autistic, and how this compares to the rest of the population. If the rate is not 2%, something is wrong with the theory or their estimation of risk.

Discern How Obesity Could Be a Cause

In this study, the authors speculate why fetal exposure to a metabolic disorder might result in adverse fetal development. They point out that poorly regulated maternal glucose (even in those not technically diabetic) leads to fetal hyperinsulinemia, which can lead to chronic hypoxia (low oxygen levels) in the fetus. This can also lead to fetal iron deficiency. They note:

Both fetal hypoxia and iron deficiency can profoundly affect neurodevelopment in humans, including alterations in myelination and cortical connectivity and aberrations in hippocampal neurons. Fetal iron deficiency has also been associated with reduced recognition memory as well as behavioral and developmental problems.

They also note that high levels of proinflammatory cytokines (common in diabetes and obesity) have been shown to disrupt normal brain development in animal studies.

All these theories are very interesting, but again, they are only speculation. You can't prove causation with speculation. Yet you know that this study is going to be used by many doctors NOW as yet another scare tactic to pressure women into losing weight before pregnancy so they can control those glucose levels and cytokines...just in case.

If a number of studies corroborates a relationship between obesity and autism, then researchers must do more than speculate about possible cause for this; they must examine it much more carefully before advising radical interventions like stringent diets or weight loss surgery. You have to know what the cause is before you can know what your cure should be, or you may inadvertently do more harm than good.

Consider Confounding and Iatrogenic Factors

Most importantly, if maternal obesity really seems to be associated with autism, then it's very important that researchers control for confounding factors, especially iatrogenic ones. In fact, obesity could simply be a surrogate marker for highly interventionist care.

For example, women of size are often placed on restricted diets or told to gain little weight (or even to lose it) during pregnancy, and we know this increases the risk for low birth-weight or SGA babies. We also know that in a number of studies, LBW/SGA babies are associated with an increased risk for autism. Are the autistic children largely limited to obese mothers with low birth-weigth/SGA babies? Or are they spread out more evenly?

In addition, women of size are rarely "allowed" to labor normally and naturally these days, with very high induction of labor rates in morbidly obese women in particular. Some research suggests that exposure to artificial pitocin during labor increases the risk for autism. No one is sure why this might be, but they speculate it could be that exogenous pitocin interferes with the natural oxytocin (love/bonding hormone) produced by babies. If there is a pitocin/autism connection, is the issue really the women's obesity or the increased amount of interventions used in their pregnancies by most doctors?

Ultrasounds are another question. Women of size are often required to get multiple ultrasounds during a pregnancy, and their ultrasounds may take longer to get an adequate image. Some experts tie ultrasounds to autism, although frankly, the evidence is very thin for this. But a supposed obesity/autism connection must also rule out increased exposure to ultrasounds as a potential "cause."

Cesareans are another intervention which has been tied to autism by some researchers. And heaven knows, morbidly obese women are subjected to a very high rate of cesareans at many institutions in this country (although many of these are probably not necessary). So again, could obesity be merely a surrogate for a pattern of obstetric over-intervention?

Sadly, NONE of these possibilities were even raised by the obesity/autism study just published. A metabolic cause was just assumed, and the possibility of confounding factors completely ignored. However, any future research into this topic MUST account for the possibility.

Final Thoughts

This study has many issues. It makes obesity a sweeping surrogate for metabolic aberrations, jumps to strong conclusions on the basis of fairly tepid data, fails to control for possible confounding factors, treats the issue far too simplistically, and tries to link a rise in autism with a rise in obesity, despite evidence that obesity is not increasing in parallel with autism.

Furthermore, this study should never have been trumpeted to the press like this. It is only the first study to find such an association, which is hardly compelling evidence. Such an association must be found in a number of studies before any serious conclusions can be made about a connection, and definitely before any major press releases are done or any radical "solutions" are proposed.

It's time for more (and better!) research on the topic, with consistent study designs between research so results can be compared more accurately. And it's time for a less mother-blaming slant to the research and publicity around it.

The language of the press releases around this study was also problematic. In the many press releasesassociated with this study, some of the interviewed doctors tried to soften the implied criticisms of obese mothers, pointing out that there was no proof (yet) that obesity causes autism and that there may be other factors at work. But just as clearly, the authors and others are using this to once again press for a weight loss agenda:

While the new research points to an association between mom's health during pregnancy and autism, it's important to note that "we can't really draw causal links," says researcher Paula Krakowiak. She is a PhD candidate in epidemiology at the University of California, Davis.
But "it is already known that any of these conditions have downstream risks in terms of pregnancy complications and delivery complications. The take-home message would be that any modifiable changes that one can make in their lifestyle or diet can benefit these conditions and potentially benefit the baby."

In another press release, commenters tell obese women not to feel guilty if they have an autistic child, while in the next breath they warn these women they may not live to see their child grow up:

While maternal obesity is linked to a modest increase in autism risk, Hyman said it can have other health consequences in mother and child. Previous studies have linked maternal obesity to birth defects, including spina bifida as well as heart and limb deformities. "Obesity is a major public health problem," she said. "The risk for autism and developmental disorders is only part of it."....

"We would not advocate treating the hypothetical causes of autism, but we would recommend women of childbearing years to eat healthy and exercise and take care of themselves, not only for the fetus but so they can see their children grow up."

See their children grow up? Even if obesity impacts lifespan, it is quite unlikely to cause mothers to die before their children grow up, and such language is pure emotionally-laden scare tactics.

Clearly, there is a strong dose of weight bias in these reports, not to mention the usual scare tactics and mother-blaming. Too bad the media wasn't more neutral in their reporting of this study.

If mother-blaming has been raised to the level of a sport in our society, then fat-mother blaming has been raised to the level of an Olympic sport.

This new study and its attendant publicity is just the latest volley in this vicious sport.

Two previous epidemiological studies of autistic twins suggested that autism was predominantly genetically determined, although the findings with regard to a broader phenotype of cognitive, and possibly social, abnormalities were contradictory. Obstetric and perinatal hazards were also invoked as environmentally determined aetiological factors. The first British twin sample has been re-examined and a second total population sample of autistic twins recruited. In the combined sample 60% of monozygotic (MZ) pairs were concordant for autism versus no dizygotic (DZ) pairs; 92% of MZ pairs were concordant for a broader spectrum of related cognitive or social abnormalities versus 10% of DZ pairs. The findings indicate that autismis under a high degree of genetic control and suggest the involvement of multiple genetic loci. Obstetric hazards usually appear to be consequences of genetically influenced abnormal development, rather than independent aetiological factors. Few new cases had possible medical aetiologies, refuting claims that recognized disorders are common aetiological influences.

OBJECTIVE: To provide the first review and meta-analysis of the association between perinatal and neonatal factors and autism risk...RESULTS: Over 60 perinatal and neonatal factors were examined. Factors associated with autism risk in the meta-analysis were abnormal presentation, umbilical-cord complications, fetal distress, birth injury or trauma, multiple birth, maternal hemorrhage, summer birth, low birth weight, small for gestational age, congenital malformation, low 5-minute Apgar score, feeding difficulties, meconium aspiration, neonatal anemia, ABO or Rh incompatibility, and hyperbilirubinemia.Factors not associated with autism risk included anesthesia, assisted vaginal delivery, postterm birth, high birth weight, and head circumference. CONCLUSIONS: There is insufficient evidence to implicate any 1 perinatal or neonatal factor in autism etiology, although there is some evidence to suggest that exposure to a broad class of conditions reflecting general compromises to perinatal and neonatal health may increase the risk. Methodological variations were likely sources of heterogeneity of risk factor effects across studies.

...METHODS: We conducted a case-control study nested within a population-based cohort (all Swedish children born in 1974-1993). We used prospectively recorded data from the Swedish Birth Register, which were individually linked to the Swedish Inpatient Register. Cases were 408 children (321 boys and 87 girls) discharged with a main diagnosis of infantile autism from any hospital in Sweden before 10 years of age in the period 1987-1994, plus 2,040 matched controls...RESULTS: The risk of autism was associated with daily smoking in early pregnancy (OR = 1.4; CI = 1.1-1.8), maternal birth outside Europe and North America (OR = 3.0; CI = 1.7-5.2), cesarean delivery (OR = 1.6; CI = 1.1-2.3), being small for gestational age (SGA; OR = 2.1; CI = 1.1-3.9), a 5-minute Apgar score below 7 (OR = 3.2, CI = 1.2-8.2), and congenital malformations (OR = 1.8, CI = 1.1-3.1). No association was found between autism and head circumference, maternal diabetes, being a twin, or season of birth. CONCLUSIONS: Our findings suggest that intrauterine and neonatal factors related to deviant intrauterine growth or fetal distress are important in the pathogenesis of autism.

...RESULTS: The risk of infantile autism was increased for mothers aged >35 years, with foreign citizenship, and mothers who used medicine during pregnancy. A higher risk of infantile autism was seen among children with low birth weight and with congenital malformations.Birth interventions, pathological cardiotocography, green amnion fluid and acidosis during delivery were not associated with increased risk for infantile autism. CONCLUSION: Our findings suggest that suboptimal birth conditions are not an independent risk factor for infantile autism. A high prevalence of lowbirth weight and birth defects among autism cases seems to explain the suboptimal birth outcome.

In this review, we provide a synopsis of work on the epidemiologic evidence for prenatal infection in the etiology of schizophrenia and autism...Some evidence also suggests that maternal infection and immune dysfunction may be associated with autism. Although replication is required, these findings suggest that public health interventions targeting infectious exposures have the potential for preventing cases of schizophrenia and autism.....

...METHOD: We studied a population-based sample of 3715 same-sex twin pairs participating in the Child and Adolescent Twin Study of Sweden (CATSS)...RESULTS: Twins lower in birth weight in ASD-discordant twin pairs (n=34) were more than three times more likely to meet criteria for ASD than heavier twins [odds ratio (OR) 3.25]. Analyses of birth weight as a continuous risk factor showed a 13% reduction in risk of ASD for every 100 g increase in birth weight (n=78)...CONCLUSIONS: The data were consistent with the hypothesis that low birth weight confers risk to ASD. Thus, although genetic effects are of major importance, a non-genetic influence associated with birth weight may contribute to the development of ASD.

...An exploratory descriptive study, utilizing retrospective chart review, was conducted to investigate the incidence of pre-, peri- and post-natal, birth and developmental problems in a sample of 1000 children with SPD and of 467 children with autism spectrum disorder(ASD), who also had SPD. This study revealed that although no one factor was strongly associated with SPD or ASD, an average of seven events for children with SPD and eight events for children with ASD occurred across categories. These included: one pre-natal/pregnancy problem, delivery complication, assisted delivery, gestational or birth-related injury/illness; one or more early childhood illnesses or injuries; two or more infancy/early childhood developmental problems; and one or more delayed early childhood developmental milestones. When comparing results to national studies of the typical population, most remarkable was the incidence of jaundice, three to four times higher in both the SPD and ASD groups than in typical children. In addition, rates of breech position, cord wrap/ prolapse, assisted delivery methods (particularly forceps and suction deliveries), and high birth-weight were greater in both groups. Incidence of premature birth was higher in the ASD although not significantly different from the SPD group. Also of note was a high frequency of absent or brief crawling phase, and high percentages of problems with ear infections, allergies, and maternal stresses during pregnancy.

...DESIGN: Subjects born in Western Australia between 1980 and 1995 and diagnosed with an autism spectrum disorder by 1999 were included as cases (n = 465). Siblings of the cases (n = 481) and a random population-based control group (n = 1313) were compared with the cases on obstetric information contained in the Maternal and Child Health Research Database of Western Australia. RESULTS: Compared with control subjects, cases had significantly older parents and were more likely to be firstborn. Case mothers had greater frequencies of threatened abortion, epidural caudal anesthesia use, labor induction, and a labor duration of less than 1 hour. Cases were more likely to have experienced fetal distress, been delivered by an elective or emergency cesarean section, and had an Apgar score of less than 6 at 1 minute. Cases with a diagnosis of autism had more complications than those with pervasive developmental disorder not otherwise specified or Asperger syndrome. Nonaffected siblings of cases were more similar to cases than control subjects in their profile of complications. CONCLUSIONS: Autism is unlikely to be caused by a single obstetric factor. The increased prevalence of obstetric complications among autism cases is most likely due to the underlying genetic factors or an interaction of these factors with the environment.

This literature review summarizes recent potential evidence, most of which is at the molecular/mechanistic level, in support of Hollander's hypothesis that excess oxytocin (OT), possibly through OT administration at birth, could contribute to the development of autistic spectrum disorders and related syndromes by proposed down regulation of the OT receptor (OTR). In this review, recent molecular evidence for OTR internalization by excess OT is related to OT's reported effects on animal social behavior, favoring social bondage, notably in sheep, voles, rats and especially mice. Adding indications for OT's capability of crossing the maternal placenta and OT's possibility of crossing an underdeveloped or stressed infantile blood brain barrier at birth, a causal connection between OT excess and behavioral disorders such as autism can be supported from a molecular perspective. Possible strategies such as a thorough statistical analysis of numerous birth records as well as molecular studies such as radiotracing using labeled OT are proposed to test this hypothesis.

Oxytocin plays an important role in social-affiliative behaviors. It has been proposed that exposure to high levels of exogenous oxytocin at birth, via pitocin induction of delivery, might increase susceptibility to autism by causing a downregulation of oxytocin receptors in the developing brain. This study examined the rates of labor induction using pitocin in children with autism and matched controls with either typical development or mental retardation. Birth histories of 41 boys meeting the criteria for autistic disorder were compared to 25 age- and IQ-matched boys without autism (15 typically developing and 10 with mental retardation). There were no differences in pitocin induction rates as a function of either diagnostic group (autism vs. control) or IQ level (average vs. subaverage range), failing to support an association between exogenous exposure to oxytocin and neurodevelopmental abnormalities.

...AIMS: To provide the first quantitative review and meta-analysis of the association between maternal pregnancy complications and pregnancy-related factors and risk of autism. METHOD: PubMed, Embase and PsycINFO databases were searched for epidemiological studies that examined the association between pregnancy-related factors and autism. Forty studies were eligible for inclusion in the meta-analysis. Summary effect estimates were calculated for factors examined in multiple studies. RESULTS: Over 50 prenatal factors have been examined. The factors associated with autism risk in the meta-analysis were advanced parental age at birth, maternal prenatal medication use, bleeding, gestational diabetes, being first born v.third or later, and having a mother born abroad. The factors with the strongest evidence against a role in autism risk included previous fetal loss and maternal hypertension, proteinuria, pre-eclampsia and swelling. CONCLUSIONS: There is insufficient evidence to implicate any one prenatal factor in autism aetiology, although there is some evidence to suggest that exposure to pregnancy complications may increase the risk.

Thursday, April 12, 2012

In the last few days, I've received about seventy gazillion emails from readers, asking me to comment on the new obesity and autism study. Yes, I'm well aware of the study and have been researching the topic for you.

My response is in the works and nearly done, but I want to take enough time to look at the topic more thoroughly than some of the press releases or commentaries I've seen so far. Add to that the fact that I'm a working mother of four who has to fit all the research and writing in between her work, Scouts, choir, school plays, illnesses, cooking, chores, and fundraising! (And that's just since Monday!)

Tuesday, April 3, 2012

Ah, the oldies-but-goodies! Funny how the same thing keeps coming up like this.

Here's yet another "Fat Vagina Theory" example from My OB Said What?!! (And people think I make this stuff up!)

"...The Fat Vaginal Walls Won't Let The Baby Pass."

"Between the Gestational Diabetes, which you obviously aren't doing the work to control, and being overweight, you'll probably get a cesarean section because the fat vaginal walls won't let the baby pass." - OB to mother prenatally

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This site is written by healthcare consumers for healthcare consumers. The information provided here is not intended as medical advice. Consult your personal healthcare providers when deciding how to use this information.